dc.contributorUniversidade Estadual de Campinas (UNICAMP)
dc.contributorUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T15:30:56Z
dc.date.available2014-05-20T15:30:56Z
dc.date.created2014-05-20T15:30:56Z
dc.date.issued2009-01-01
dc.identifierNeuroimmunomodulation. Basel: Karger, v. 16, n. 1, p. 54-62, 2009.
dc.identifier1021-7401
dc.identifierhttp://hdl.handle.net/11449/40213
dc.identifier10.1159/000179667
dc.identifierWOS:000261830400007
dc.description.abstractMost reports of autoimmune response during infection with the parasite Trypanosoma cruzi have dealt with the cardiomyopathic form of Chagas' disease, but little is known about the mechanisms of tissue damage involved in the gastrointestinal form, which was studied here. Chronically infected patients with a severe gastrointestinal form of Chagas' disease present increased antibody production and proliferative responses to peripheral myelin components, such as myelin basic protein (MBP), which is homologous to the P1 protein fraction of peripheral myelin. T lymphocytes preferentially recognize a region on the MBP molecule (1-30), which suggests that the MBP is a potential target on the peripheral nerve for autoimmune reactions in patients with gastrointestinal lesions resulting from Chagas' disease. Copyright (C) 2008 S. Karger AG, Basel
dc.languageeng
dc.publisherKarger
dc.relationNeuroimmunomodulation
dc.relation2.238
dc.relation1,064
dc.rightsAcesso restrito
dc.sourceWeb of Science
dc.subjectMyelin basic protein
dc.subjectAutoimmunity
dc.subjectTrypanosoma cruzi
dc.titleNeuropathy of Gastrointestinal Chagas' Disease: Immune Response to Myelin Antigens
dc.typeArtículos de revistas


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